ArticleCellular microbiology2010
E. coli secreted protein F promotes EPEC invasion of intestinal epithelial cells via an SNX9-dependent mechanism.
Article in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Oral Administration with Live Attenuated Citrobacter rodentium Protects Immunocompromised Mice from Lethal Infection.Infection and immunity · 2022Article
- Safeguarding intestine cells against enteropathogenicProceedings of the National Academy of Sciences of the United States of America · 2020Article
- EnteropathogenicInternational journal of molecular sciences · 2020Article
- EspF is crucial for Citrobacter rodentium-induced tight junction disruption and lethality in immunocompromised animals.PLoS pathogens · 2019Article
- Chlamydia exploits filopodial capture and a macropinocytosis-like pathway for host cell entry.PLoS pathogens · 2018Article
- Clever Cooperation: Interactions Between EspF and Host Proteins.Frontiers in microbiology · 2018Review
- EPEC effector EspF promotes Crumbs3 endocytosis and disrupts epithelial cell polarity.Cellular microbiology · 2017Article
- Endocytosis, Metastasis and Beyond: Multiple Facets of SNX9.Trends in cell biology · 2017Review
- The Bacterial SpeciesFrontiers in microbiology · 2017Article
- Escherichia albertii, a novel human enteropathogen, colonizes rat enterocytes and translocates to extra-intestinal sites.PloS one · 2017Article
- Tight Junction Disruption Induced by Type 3 Secretion System Effectors Injected by Enteropathogenic and Enterohemorrhagic Escherichia coli.Frontiers in cellular and infection microbiology · 2016Review
- Core 2 mucin-type O-glycan inhibits EPEC or EHEC O157:H7 invasion into HT-29 epithelial cells.Gut pathogens · 2015Article
- Enteropathogenic E. coli effectors EspG1/G2 disrupt microtubules, contribute to tight junction perturbation and inhibit restoration.Cellular microbiology · 2014Article
- Actin cytoskeleton manipulation by effector proteins secreted by diarrheagenic Escherichia coli pathotypes.BioMed research international · 2013Review
- The N-terminal domain of EspF induces host cell apoptosis after infection with enterohaemorrhagic Escherichia coli O157:H7.PloS one · 2013Article
- A pathogen's journey in the host cell: Bridges between actin and traffic.Bioarchitecture · 2012Article
- Always one step ahead: How pathogenic bacteria use the type III secretion system to manipulate the intestinal mucosal immune system.Journal of inflammation (London, England) · 2011Article
- Genome sequence of adherent-invasive Escherichia coli and comparative genomic analysis with other E. coli pathotypes.BMC genomics · 2010Article
- The EspF effector, a bacterial pathogen's Swiss army knife.Infection and immunity · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Enteropathogenic Escherichia coli (EPEC) infection requires the injection of effector proteins into intestinal epithelial cells (IECs) via type 3 secretion. Type 3-secreted effectors can interfere with IEC signalling pathways via specific protein-protein interactions. For example, E. coli secreted protein F (EspF) binds sorting nexin 9 (SNX9), an endocytic regulator, resulting in tubulation of the plasma membrane. Our aim was to determine the mechanism of EspF/SNX9-induced membrane tubulation. Point mutation of the SNX9 lipid binding domains or truncation of the EspF SNX9 binding domains significantly inhibited tubulation, as did inhibition of clathrin coated pit (CCP) assembly. Although characterized as non-invasive, EPEC are known to invade IECs in vitro and in vivo. Indeed, we found significant invasion of Caco-2 cells by EPEC, which, like tubulation, was blocked by pharmacological inhibition of CCPs. Interestingly, however, inhibition of dynamin activity did not prevent tubulation or EPEC invasion, which is in contrast to Salmonella invasion, which requires dynamin activity. Our data also indicate that EPEC invasion is dependent on EspF and its interaction with SNX9. Together, these findings suggest that EspF promotes EPEC invasion of IECs by harnessing the membrane-deforming activity of SNX9.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.